We have used a partially purified toxin from the
venom of the brown recluse spider, Loxosceles reclusa, to study its effects on human platelets isolated from
plasma proteins. This toxin, which produced skin
necrosis in rabbits, contained
sphingomyelinase D activity. The toxin induced platelet aggregation and secretion of [3H]
serotonin in human plasma but not in
buffer or in human neonate plasma. Ca2+ was required for the interaction of toxin, platelets, and plasma factor(s). The addition of
C-reactive protein restored aggregation and
serotonin release of platelets incubated in human neonate plasma. The
ADP-degrading
enzyme,
apyrase, and the non-steroidal, anti-inflammatory
drug,
indomethacin, inhibited platelet aggregation, suggesting that
ADP secreted from platelet storage granules and
indomethacin-sensitive pathway(s) are involve in the toxin-induced human platelet activation (aggregation and
serotonin release). Generation of
platelet activating factor (PAF) from the platelet by brown recluse toxin is not likely since the PAF receptor antagonist,
BN 52021, did not inhibit platelet aggregation induced by the brown recluse toxin.